The aim of this study is to determine if the sympathetic nervous system either directly or indirectly via circulating catecholamines regulates pathophysiological states associated with massive histamine release. This investigation will attempt to specifically determine the role of catecholamines in modifying increases in microvascular permeability to plasma proteins, functional changes in microvascular surface area via beta-adrenergic receptors, and determine under what conditions these effects could be of physiological importance. This will be accomplished by measuring changes in transvascular fluid and protein transfer in skin, skeletal muscle, and intestine in mongrel dogs anesthetized with pentobarbital. In each organ studied, weight, vascular pressures and flows, flow and protein concentration of the lymph will be measured and the capillary filtration coefficients will be calculated. The effects of exogenous and endogenous catecholamines and local and generalized sympathetic nerve stimulation on protein efflux by locally and systemically infused histamine and bradykinin will be investigated to determine the mechanism and possible physiological importance of the antagonism by catecholamines to the protein efflux produced by these two edemogenic agents. The effects of cooling on transvascular protein transfer will be studied to determine the relative contributions of large pores and micropinocytosis on protein transfer normally and during the local infusion of histamine and bradykinin. The capillary filtration coefficients will be calculated during physiologically-induced reflex sympathetic nerve activation both before and after beta-receptor blockade to determine if sympathetic stimulation also alters functional microvascular surface area via beta-adrenergic receptors. These data will have relevance to basic physiologic control mechanisms affecting microvascular protein transfer and surface area normally and in circulatory shock states.